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Like other primary musculoskeletal tissues, bone is comprised of mesenchymal cells embeddedwithin an extracellular matrix. However, unlike other secreted matrices, bone matrix containsmineral (calcium) that gives the tissue great strength and stiffness in compression and bending.The organic component in bone, primarily type I collagen, gives bone its ability to withstandgreat tension. Bone is also equipped with an elaborate blood, nerve, and lymphatic supply. Theperiosteum covers the external surfaces of bone and plays a fundamental role in the healing offractures. Human bones consist of two forms of bone tissue: cortical (compact) bone and cancellous(spongy) bone. FRACTURE HEALING A bone fracture initiates a response sequence of inflammation, repair, and remodelling to restorethe injured bone to its original state. Inflammation begins immediately after injuryoccurs and is followed rapidly by repair.
After repair has replaced the lost and damaged cellsand matrix, a prolonged remodelling phase begins (Paton, 1992). INFLAMMATION First, a haematoma accumulates within the medullary canal between the fracture ends andbeneath the elevated periosteum. An injury that fractures bone does not only damage the cells,blood vessels, and bone matrix, but also the surrounding soft tissues (including periosteum andmuscle) contributing necrotic material to the fracture site. Inflammatory mediators, released from platelets and from dead and injured cells, dilate bloodvessels and excrete plasma. This leads to the acute edema seen in the region of a freshfracture (Sarmiento and Latta, 1995). Inflammatory cells, such as leukocytes followed bymacrophages and lymphocytes, migrate to the region. As the inflammatory response subsides,necrotic tissue and plasma are reabsorbed as fibroblasts appear to begin producing a newmatrix. REPAIR Osteoclasts, derived from circulating monocytes and local bone marrow, reabsorb the necroticbone cells near the fracture site. Disruption of blood vessels in the bone, periosteum, marrow,and surrounding tissue due to injury results in collateral sprouting of nearby blood vessels.Invasion of the haematoma by these new capillary loops forms organised granulation tissuewithin which fibroblasts proliferate (Williams, 1985). The primitive bone cells give rise tochondroblasts and osteoblasts.
The chondroblasts secrete phosphotase, an enzyme promotingthe deposition of calcium, to form a bridge of callus. The bone formed initially at the periphery ofthe inflammatory reaction is called the hard callus. The new tissue formed in the centre of theinflammatory reaction is primarily cartilage and is called the soft callus (Apley, 1982).Osteoblasts then grow into the bridge and into the tissue between the fractured ends of thebone by endochondral ossification, replacing the callus with a network of woven (immature) bone. REMODELLING During the final stages of repair, the woven bone is replaced by lamellar (mature) bone andosteoclasts reabsorb unneeded callus. This process often goes on long after the patient has fullrestoration of function and complete bone union has been demonstrated (Apley, 1982). The endresult of remodelling is bone that, even if it has not been returned to its original form, has beenaltered to perform the function demanded of it. Ultimately, the important functional result for thepatient is an increase in mechanical stability from the end of the repair phase. VARIABLES THAT INFLUENCE FRACTURE HEALING Sometimes fractures take longer to heal in certain patients. These differences can usually beexplained by variations in the patient, the type of injury, and the location of injury.
Patient Variables Age is among the most important patient variables that influence fracture healing. Most fracturesin children heal rapidly. Periosteal cells have an especially prominent role in healing children’s fractures because the periosteum is thicker and more cellular in younger individuals (Wiesel andDelahay, 1997). With increasing age, the periosteum becomes thinner and its contribution tofracture healing becomes less apparent. In addition, the rapid bone remodelling thataccompanies growth allows correction of a greater degree in children. A variety of hormones can influence the rate of fracture healing. Corticosteroids, for example,compromise fracture healing, possibly by inhibiting the differentiation of osteoblasts frommesenchymal cells and by decreasing synthesis of organic bone matrix components necessaryfor repair (Wiesel and Delahay, 1997). Other hormones naturally present in the body can alsoeither speed up or slow down the rate of repair. Injury Variables The severity of a fracture can have a formidable influence on the healing of the wound.Displacement of the fracture fragments and severe trauma to the soft tissues retard fracturehealing, probably because the extensive tissue damage increases the amount of necrotic tissueand haematoma and impedes proliferating blood vessels and migrating mesenchymal cells(Wiesel and Delahay, 1997).
Normally, healing proceeds from both sides of a fracture, but if onefracture fragment has lost its blood supply, healing depends entirely on ingrowth of capillariesfrom the living side. If a fracture fragment is avascular the fracture can heal, but the rate isslower and the incidence of healing is lower than if both fragments have a normal blood supply.Open fractures present the same problems of soft tissue disruption and fracture displacement,but they also can involve significant bone loss and infection. If an infection does occur following fracture, many cells must be diverted to attempt to eliminateit. This slows down the rate of repair because there are fewer cells devoted primarily to healingthe fracture. Furthermore, infection may cause necrosis of normal tissue, edema, andthrombosis of blood vessels, thereby retarding or preventing healing. Interposition of soft tissue including muscle, fascia, tendon, and occasionally nerves and bloodvessels between fracture fragments will compromise fracture healing. In these circumstances,the tissue must be extricated to reposition the fracture fragments (Wiesel and Delahay, 1997). Variables in the Location of Injury Intra-articular fractures are sometimes slower in healing because of the presence of collagenase in synovial fluid that can degrade the matrix of the initial fracture callus and thereby retard thefirst stage in fracture healing (Wiesel and Delahay, 1997).
Healing of cancellous and cortical bone fractures differs because of the differences in surfacearea, vascularity, and cellularity. Opposed cancellous bone surfaces usually unite rapidlybecause the large surface area per unit volume of cancellous bone creates many points ofcontact for cells and blood supply and because osteoblasts will form bone directly on existingtrabeculae (Williams, 1985). Where fractured cancellous bone surfaces are not in contact, newbone spreads from the points of contact to fill the gaps. In contrast, cortical bone has a muchsmaller surface area per unit volume and generally a less extensive internal blood supplythereby making it more difficult to heal. The repair phase differs between fractures occurring in the metaphyses (primarily cancellousbone) and fractures occurring in the diaphyses (primarily cortical bone). Metaphyseal blood flowis more abundant than diaphyseal flow and increases when a fracture occurs (Sarmiento andLatta, 1995).
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